PMID- 16454731
OWN - NLM
STAT- MEDLINE
DCOM- 20060222
LR  - 20190728
IS  - 1381-6128 (Print)
IS  - 1381-6128 (Linking)
VI  - 12
IP  - 2
DP  - 2006
TI  - The dendritic cell-T cell synapse as a determinant of autoimmune pathogenesis.
PG  - 131-47
AB  - Autoimmune diseases occur when the immune response is targeted to self-antigens, 
      leading to destruction or altered function of specific cells and tissues. 
      Although the aetiology of these diseases has not yet been fully elucidated, it is 
      believed that genetically determined susceptibility and environmental triggers 
      are both implicated in the detrimental immune response against the body's own 
      tissues. Dendritic cells (DCs) are professional antigen presenting cells that 
      play an important role in maintaining peripheral tolerance by preventing 
      self-reactive T cells from causing autoimmune damage. Thus, alterations in the 
      physiology of DCs are likely to be responsible for defective immune regulatory 
      mechanisms and incomplete tolerance to self. Here, we will focus specifically on 
      the ways in which the immunological synapse occurring at the DC-T cell interface 
      can fine-tune the balance between tolerance and immunity and how alterations of 
      this synapse can determine induction or perpetuation of autoimmune responses. 
      Activating/inhibitory receptors expressed on the surface of DCs and T cells 
      modulate the function of these cells and influence the course of the immune 
      response. Pharmacological approaches that can modulate DC function will be also 
      addressed as a potential antigen-specific strategy in the design of new, 
      noninvasive therapies to prevent or to treat chronic inflammatory autoimmune 
      disorders.
FAU - Iruretagoyena, Mirentxu I
AU  - Iruretagoyena MI
AD  - Departamento de Genetica Molecular y Microbiologia, Facultad de Ciencias 
      Biologicas, Pontificia Universidad Catolica de Chile.
FAU - Wiesendanger, Margrit
AU  - Wiesendanger M
FAU - Kalergis, Alexis M
AU  - Kalergis AM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - Curr Pharm Des
JT  - Current pharmaceutical design
JID - 9602487
RN  - 0 (Receptors, Antigen, T-Cell)
SB  - IM
MH  - Animals
MH  - Autoimmune Diseases/drug therapy/*immunology/physiopathology
MH  - Cell Communication/drug effects/*immunology
MH  - Dendritic Cells/drug effects/*immunology/physiology
MH  - Humans
MH  - Immune Tolerance
MH  - Receptors, Antigen, T-Cell/drug effects/immunology/physiology
MH  - T-Lymphocytes/drug effects/*immunology/physiology
RF  - 189
EDAT- 2006/02/04 09:00
MHDA- 2006/02/24 09:00
CRDT- 2006/02/04 09:00
PHST- 2006/02/04 09:00 [pubmed]
PHST- 2006/02/24 09:00 [medline]
PHST- 2006/02/04 09:00 [entrez]
AID - 10.2174/138161206775193145 [doi]
PST - ppublish
SO  - Curr Pharm Des. 2006;12(2):131-47. doi: 10.2174/138161206775193145.